Learning Objectives: Basic knowledge about the anatomy and function of the mastoid provides a rationale for obliteration of the cavity in cholesteatoma surgery.
“Danish Otology Society symposium”
Mastoidectomy is often included in cholesteatoma surgery in order to eradicate the disease. In such cases the subsequent reconstruction of the middle ear may include obliteration of the mastoid. This has become increasingly popular, because studies have demonstrated less recurrent cholesteatomas. While this may speak for itself, the basic reasons for obliteration have not been documented.
The rationale for mastoid obliteration should be based on its function in normal and diseased ears, but our understanding of the mastoid function is rather limited despite its unique structure compared with the tympanum. Thus, the mastoid has been regarded to have only a passive role, where it may enhance the area for gas exchange as well as be a pressure buffer by virtue of its volume.
Recent clinical physiological experiments have demonstrated how pressure regulation of the middle ear cleft consists of both stepwise pressure changes by Eustachian tube openings as well as gradual pressure changes explained by changes in the thickness or congestion of the mastoid mucosa. More studies have confirmed this idea, which may point to a role of the mastoid in the overall pressure regulation.
The histological structure of the mastoid mucosa favors such a function by a loose connective tissue and abundant blood vessels. However, the mucosa does not display cilia and goblet cells as found in the tympanum, which makes it more susceptible to inflammatory changes. Chronic or recurrent infections may easily cause a relative fibrosis, which inevitably limits its capability for thickness changes based on its congestion, whereas its capability for gas absorption may remain unaffected.
In this scenario, the mastoid mucosa may have lost its functional properties because of chronic or recurrent inflammations, and obliteration can eliminate the contribution of a diseased mucosa, which may contribute only to gas absorption and development of middle ear underpressure.
